Kumari Anshu (PhD Scholar) presented her ongoing PhD work entitled "Prenatal Valproic Acid exposure in rats: The neural mechanism of changes in attention".
Kumaresan UD (MPhil Scholar) presented the paper by Zhan et al in Nature Neuroscience entitled "Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior"
Microglia are phagocytic cells that infiltrate the brain during development and have a role in the elimination of synapses during brain maturation. Changes in microglial morphology and gene expression have been associated with neurodevelopmental disorders. However, it remains unknown whether these changes are a primary cause or a secondary consequence of neuronal deficits. Here we tested whether a primary deficit in microglia was sufficient to induce some autism-related behavioral and functional connectivity deficits. Mice lacking the chemokine receptor Cx3cr1 exhibit a transient reduction of microglia during the early postnatal period and a consequent deficit in synaptic pruning. We show that deficient synaptic pruning is associated with weak synaptic transmission, decreased functional brain connectivity, deficits in social interaction and increased repetitive-behavior phenotypes that have been previously associated with autism and other neurodevelopmental and neuropsychiatric disorders. These findings open the possibility that disruptions in microglia-mediated synaptic pruning could contribute to neurodevelopmental and neuropsychiatric disorders.
Kumari Anshu Jha (2nd year PhD scholar) presented her seminar on "Interneuron dysfunction in neuropsychiatric disorders". She focused on GABAergic dysfunction in Schizophrenia and Autism.
Anshu gave an overview of Interneuron functions (feedback & feedforward inhibition, network oscillations and synchrony, modulation of excitability, integration and cortical development and plasticity) and then highlighted the complexity of internuron types (classified based on morphological, molecular, electrophysiological properties - eg Markram 2004).
She then discussed the role of GABAergic neurons in the pathophysiology of Schizophrenia and then Autism from post-mortem studies and animal models (gene knockouts) while showing that GABA impairment seems to be present in a wide variety of neuropsychiatric disorders. She then went through the mechanisms through which these interneurons modulate network oscillations via electrical gap junctions and neurochemical modulations amongst the interneurons (for example Parvalbumin expressing basket cells impact gamma oscillations while somatostatin expressing interneurons impact beta oscillations).
Considering that the type of impairment is similar for schizophrenia and autism, the timing of the impairment seems to be a differentiator between these two disorders. Autism is seen in early childhood (diagnosed around 3 years of age when neuronal pruning is still ongoing) and the first onset of Schizophrenia happens in adolescence (when the neurons are fully formed but the myelination is still an ongoing process).